期刊
CELL AND TISSUE RESEARCH
卷 306, 期 1, 页码 57-63出版社
SPRINGER-VERLAG
DOI: 10.1007/s004410100420
关键词
alveolar type II cells; gene regulation; in situ hybridization; lung injury; wound healing; mutant mice (C/EBP alpha-deficient)
类别
The lung-specific surfactant proteins (SP) are essential for normal respiratory function. Transcription factors may play an important role in the regulation of surfactant proteins. The CCAAT/enhancer-binding protein (C/EBP) family consists of transcription factors that can stimulate expression of genes in lipid-metabolizing epithelial cells. C/EBP alpha -deficient mice have been shown to exhibit abnormal pulmonary histopathology. Recently, we demonstrated that C/EBP family members are differentially expressed in alveolar type II cell proliferation and in pulmonary fibrosis. In the present study, to investigate whether the C/EBP family would be involved in the regulation of surfactant proteins, we examined the protein expression of SP-A, and SP-C, and mRNA expression of SP-A, SP-B, and SP-C in the lungs from newborn C/EBP alpha -deficient mice. Using immunohistochemistry, we demonstrated that positive cells for SP-C, specific to alveolar type II cells, in the lungs were more abundant in the newborn C/EBP alpha -deficient mice than in control mice, which suggests the hyperproliferation of alveolar type II cells in the lungs of the C/EBP alpha -deficient mice. In situ hybridization analysis revealed that expression of SP-A, SP-B, and SP-C mRNAs were increased in the lungs of newborn C/EBP alpha -deficient mice. Northern blot analysis revealed that surfactant protein mRNAs were also increased. Thus, these results suggest that C/EBP alpha may play a key role in the proliferation of alveolar type II cells and the regulation of genes of surfactant protein.
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